Cutaneous wound healing consists of an orderly series of events, whose goal is the re-establishment of tissue integrity and function. However, its misregulation can lead to chronic wounds or to hyperproliferative disorders. One model that successfully mimics many aspects of normal wound healing, including tissue contraction, matrix metalloproteinase (MMP) induction, and apoptosis, involves culturing fibroblasts within three- dimensional collagen gels. Although FAK plays a major role in regulating fibroblast functions such as cytoskeletal rearrangements, cell migration and survival, its role in dermal wound repair has not been defined. Our preliminary data indicates that FAK-deficient murine cells are virtually unable to contract gels, but hyper-express MMP-13. These data indicate that FAK activity, or its inactivation, likely plays an important role in regulating wound healing processes. Therefore, I propose to: 1) determine the mechanism by which FAK promotes collagen gel contraction, 2) test the hypothesis that FAK is inactivated following gel contraction and that this permits upregulation of MMP-13 expression, 3) determine whether FAK inactivation is important for triggering apoptosis in fibroblasts following collagen gel contraction.